Current Pharmaceutical Biotechnology - Online First

Selenium is an important trace element that plays crucial roles in metabolism, immune function, and antioxidant defense. As an antioxidant, selenium helps to alleviate postpartum uterine inflammation and promotes uterine recovery. However, the exact mechanism underlying the role of selenium in postpartum uterine recovery is not fully understood.

This study aimed to identify the underlying mechanism and examine how selenium enhances postpartum uterine healing.

Female ICR mice aged 8 weeks were classified into five groups: control, postpartum model, low-dose selenium (100 nm), medium-dose selenium (200 nm), and high-dose selenium (400 nm). Endometrial morphology was evaluated by hematoxylin and eosin (H&E) staining. Oxidative stress markers, including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), and malondialdehyde (MDA), and inflammatory factors, including tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β), were measured using commercially available kits. GPX1, GPX4, and nuclear factor erythroid 2-related factor 2 (NRF2) expression were determined using real-time PCR and WB.

We found damage and bleeding points in the endometrium and destruction of the ultrastructure of endometrial cells in the postpartum model group; however, mice treated with a high dose (400 nm) of selenium showed alleviated levels of pathological alteration in the endometrium. In addition, the levels of MDA in the postpartum mice group increased, while the SOD, CAT, and GPX levels decreased; however, changes in these oxidative stress markers were reversed after selenium treatment. For inflammatory factors, high levels of TNF-α and IL-1β were observed in postpartum mice, whereas they were decreased in selenium-treated groups. GPX1, GPX4, and NRF2 expression were reduced in postpartum model mice, but upregulated in selenium-treated mice.

Selenium supplementation ameliorated postpartum uterine oxidative stress and inflammation and promoted uterine recovery via the GPX1/GPX4/NRF2 pathway in mice.

Metabolic syndrome encompasses conditions such as diabetes mellitus (DM), which has become increasingly prevalent. Chemically synthesized medications are commonly used to mitigate the effects of DM and its complications; however, these often result in undesirable side effects, including weight gain, digestive issues, and heart failure.

This review highlights the therapeutic potential of bioactive compounds and anti-diabetic plants that possess proven anti-diabetic properties. Focusing on phytomedicines also explores their possible mechanisms of action and positions this work relative to current reviews in the field.

A comprehensive literature analysis was conducted, emphasizing the therapeutic potential of bioactive compounds in anti-diabetic plants. Databases such as PubMed, Scopus, and Google Scholar were thoroughly searched to identify studies investigating the anti-diabetic properties and mechanisms of action of plant-derived bioactive compounds. Inclusion criteria focused on studies evaluating the pharmacological effects of herbal medicines, plant extracts, and isolated bioactive compounds on diabetes management.

Therapeutic plants, as sources of anti-diabetic compounds, offer significant advantages. They are affordable, exhibit minimal or no adverse effects, and do not necessitate strict dietary restrictions or intense exercise regimens. The integrated insights underscore the potential of phytomedicines to address limitations in current diabetes management strategies.

The unique focus on phytomedicines positions this review as a valuable resource for researchers and clinicians. Detailing mechanisms and evidence supporting the efficacy of these compounds, guides the development of innovative strategies for identifying and utilizing bioactive compounds in effective diabetes management.

Bibliometrics has been applied to the study of tumor image segmentation, which can indicate the current research hotspots and trends.

In this study, bibliometric analyses were performed on data retrieved from the Web of Science database. A total of 3,377 articles on the application of tumor image segmentation from January 1, 2003, to October 9, 2024, were analyzed for the characteristics of the articles, including the number of yearly publications, country/region, institution, journal, author, keywords, and references. Visualising co-authorship, co-citation, and co-occurrence analysis with VOSviewer.

The annual publication volume of tumor image segmentation literature shows that from the first time of more than 100 articles in 2016, the publication volume of literature in this field has surged, reaching 576 articles by 2023. Mainland China is ranked first in terms of publication volume (n=1,356). Saudi Arabia ranks first in average publication year (n=2021.96). IEEE Transactions on Medical Imaging was the journal with the highest average number of citations. The Chinese Academy of Sciences (n=78) was the most prolific institution, while Harvard University was the most prestigious, with a total number of citations and an average number of citations of 3,190 and 213, respectively. In terms of keywords, co-occurrence analysis of 107 keywords with a frequency of more than 30 times produced four clusters: (1) methods of image segmentation, (2) applications of image segmentation, (3) image segmentation modelled on CT, (4) image segmentation modelled on MRI. Transformer, Attention Mechanism, and U-Net are the latest keywords. The analysis of keywords helps scholars understand and identify the current research hotspots and research directions.

Within the last 20 years, the number of articles on the application of tumor image segmentation has increased steadily. From U-Net to MAMBA, many methods for tumor image segmentation have been proposed, and the limitations of models and algorithms are becoming increasingly smaller, which demonstrates the importance of advances in tumor image segmentation technology for disease prevention and monitoring. It presents a strong connection between countries/regions and authors, which reflects the global interest and labelport for the development of this field. This study shows global trends, research hotspots, and emerging topics in this field and reviews some of the knowledge about tumor image segmentation applications from past studies. And it will provide good research guidelines for researchers in this field.

T-cell exhaustion (TEX) is one reason for immunotherapy resistance among cancers, but the specific mechanism and influencing factors of TEX in diffuse large B-cell lymphoma (DLBCL) are not fully understood. This study aimed to establish a TEX signature for predicting the prognosis of DLBCL and investigate the immune characteristics related to the TEX signature.

The gene expression data of DLBCL were obtained from The Cancer Genome Atlas and Gene Expression Omnibus databases. Prognostic TEX related genes were selected by Cox regression analysis for prognostic signature (TEX score) construction. The correlation of risk grouping with immune cell infiltration was analyzed by CIBERSORT and ssGSEA. Molecular mechanisms between high and low TEX score groups were explored by gene set enrichment analysis (GSEA).

A total of 115 differentially expressed TEX-related genes were selected, and 12 were prognosis-related after Cox regression. Following Ninesignature genes, including TRIM6, BIRC3, CTSC, GBP3, IRF3, TRIM22, IFI30, TRIM25 and BAG4 were identified to construct a TEX score. The receiver operator characteristic curve curves suggested that the model presented high predictive precision. A nomogram was established, which also had good prediction performance in survival prognosis. The composition of immune cells in the two risk groups was significantly different. GSEA identified 33 hallmarks between two risk groups, which were associated with immune cells infiltration and inflammation.

The TEX score has prognosis-predicting value for DLBCL and might be a valuable biomarker to guide clinical decision‐making for patients with DLBCL.

Diet-related chronic diseases, such as cardiovascular diseases, obesity, diabetes, autoimmune diseases and cancer, are largely preventable with a healthy diet and lifestyle. Therefore, searching for dietary supplements rich in antioxidant and anti-inflammatory phytochemicals for the prevention and/or management of diet-related chronic diseases is an important strategy for controlling these diseases to reduce healthcare costs and sustain development.

The aim of the current research was to prepare dietary supplements from avocado fruit pulp [AFPDS] and evaluate their potential against various diet-related chronic diseases through in-vitro , in-vivo , and molecular docking studies.

Volatile compounds of avocado pulp were evaluated, and the total phenolic compounds, fatty acids, and phytosterols profiles of the AFPDS were determined.

D-limonene, methyl propanoate, isobutyl propanoate and pentanol were the principal volatile compounds in the avocado pulp. Total phenolic and flavonoids were present in the AFPDS by 9.65 mg GAE/g and 6.87 mg CE/g, respectively. Chlorogenic acid and cinnamic acid were the major and minor identified phenolic compounds in AFPDS, respectively. Oleic acid [75.06%] and β-Sitosterol [2.19%] were the highest fatty acid and phytosterol present in AFPDS, respectively. AFPDS recorded anti-inflammatory activity against nitric oxide [NO] production in RAW264.7 macrophages by 98.2µg/ml [IC50] and 164.8µg/ml [IC90]. AFPDS showed significant anti-inflammatory activity against carrageenan-induced rat paw edema. AFPDS showed antioxidant activity against DPPH and ABTS by 8.67 mg TE/g and 6.14 mg TE/g. AFPDS possessed anti-cancer activity against MCF7 and HPG2 at10.8µg/ml and 40.5µg/ml, respectively. AFPDS exhibited anti-diabetic activity as an inhibitor of α-amylase and α-glucosidase by26.35±0.77μg/ml and 0.55±0.163mg/ml, respectively. Molecular docking studies revealed high binding affinity of different active compounds present in AFPDS with cyclooxygenase-2, glutathione peroxidase, α-glucosidase and B-cell lymphoma-extra-large proteins.

AFPDS can be considered a new agent for the prevention and treatment of diet-related chronic diseases, such as diabetes and cancer, due to its anti-inflammatory, antioxidant, anticancer, and anti-diabetic activities, as demonstrated through in-vivo , in-vitro , and molecular docking studies.

Atherosclerosis (AS) is caused by the endothelium injury associated with oxidative stress. Previous studies have shown that the Phlegm-Eliminating and Stasis-Transforming Decoction (Huayu Qutan Decoction, HYQTD) has mitochondrial protective function. The objective of this research was to explore how HYQTD drug-containing serum (HYQTD-DS) could potentially protect mitochondrial energy production in endothelial cells (ECs) from injury caused by hydrogen peroxide (H2O2)-induced oxidative damage in AS through SIRT1/PGC-1α/ Nrf2 pathway.

After preparation of containing serum, the cells were divided into various categories, such as control group, H2O2 group (an oxidative damage model), HYQTD group, Selisistat (EX527, a SIRT1 inhibitor) combined with H2O2 group, and EX527 combined with HYQTD group. The evaluation of oxidative stress involved measuring reactive oxygen species (ROS) and malondialdehyde (MDA) generation, as well as Superoxide Dismutase (SOD) activity. Mitochondrial function and ultrastructure were measured by Transmission electron microscopy (TEM), mitochondrial membrane potential (MMP), rate of oxygen consumption (OCR), respiratory chain complex activities, and ATP production. The key proteins and gene levels in the SIRT1/PGC-1α/Nrf2 pathway was quantified by quantitative real-time PCR (RT-PCR) and Western blotting analysis.

We found oxidative stress, mitochondrial damage, and mitochondrial energy disorder in H2O2-induced ECs. However it indicated a marked reversal after pretreated with HYQTD-DS. Mechanistically, EX527 induced increased oxidative stress, worse mitochondrial dysfunction, and less ATP synthesis.

We demonstrated that HYQTD-DS attenuated oxidative stress, improved mitochondrial function, and up-regulated mitochondrial ATP synthesis by activating SIRT1/PGC-1α/Nrf2 pathway-induced mitochondrial biogenesis and its downstream NADH dehydrogenase (ubiquinone) flavoprotein 2 (NDV2).